The DOI matches its Crossref record; 27 of the 27 references it cites were found in a registry or an index.
Chronic inhibition of glutamate uptake produces a model of slow neurotoxicity.
Open accessAbstract
Defects in neurotransmitter glutamate transport may be an important component of chronic neurotoxicity in diseases such as amyotrophic lateral sclerosis. There are no reliable models of slow glutamate neurotoxicity. Most previous in vitro systems have studied the rapid neurotoxic effects of direct-acting glutamate agonists. Therefore, we developed a model of slow toxicity in cultured organotypic spinal cord slices. The model was based on selective inhibition of glutamate transport, which continuously raised the concentration of glutamate in the culture medium. This resulted in the slow degeneration of motor neurons over several weeks. Motor neuron toxicity was selectively prevented by non-N-methyl-D-aspartate glutamate receptor antagonists and glutamate synthesis or release inhibitors but not by N-methyl-D-aspartate receptor antagonists. Thus, selective inhibition of glutamate transport produces a model of clinically relevant slow neurotoxicity and appears to be mediated by the action of non-N-methyl-D-aspartate receptors. This data supports the hypothesis that the slow loss of motor neurons in amyotrophic lateral sclerosis could be due, in part, to defective glutamate transport.
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A simple method for organotypic cultures of nervous tissue
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A rapid radiochemical method for the determination of choline acetyltransferase
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Excitatory amino acid neurotoxicity and neurodegenerative disease
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Decreased Glutamate Transport by the Brain and Spinal Cord in Amyotrophic Lateral Sclerosis
Rothstein, J. D., Martin, L. J., & Kuncl, R. W. (1992) · New England Journal of Medicine · doi:10.1056/nejm199205283262204 · Cited by 1,177
Self-citationAbnormal excitatory amino acid metabolism in amyotrophic lateral sclerosis
Rothstein, J. D., Tsai, G., Kuncl, R. W., Clawson, L., Cornblath, D. R., Drachman, D. B., Pestronk, A., Stauch, B. L., & Coyle, J. T. (1990) · Annals of Neurology · doi:10.1002/ana.410280106 · Cited by 636
Self-citationHertz, L. (1979) · Progress in Neurobiology · doi:10.1016/0301-0082(79)90018-2 · Cited by 628
AMPA glutamate receptor subunits are differentially distributed in rat brain
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GLUTAMATE-INDUCED NEURONAL NECROSIS IN THE INFANT MOUSE HYPOTHALAMUS: An Electron Microscopic Study
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Cited by
Oxidative Stress, Glutamate, and Neurodegenerative Disorders
Coyle, J. T., & Puttfarcken, P. (1993) · Science · doi:10.1126/science.7901908 · Cited by 3,762
Rothstein, J. D., Dykes-Hoberg, M., Pardo, C. A., Bristol, L. A., Jin, L., Kuncl, R. W., Kanai, Y., Hediger, M. A., Wang, Y., Schielke, J. P., et al. (1996) · Neuron · doi:10.1016/s0896-6273(00)80086-0 · Cited by 2,534
Self-citationOligodendroglia metabolically support axons and contribute to neurodegeneration
Lee, Y., Morrison, B. M., Li, Y., Lengacher, S., Farah, M. H., Hoffman, P. N., Liu, Y., Tsingalia, A., Jin, L., Zhang, P.-W., et al. (2012) · Nature · doi:10.1038/nature11314 · Cited by 1,664
Self-citationβ-Lactam antibiotics offer neuroprotection by increasing glutamate transporter expression
Rothstein, J. D., Patel, S., Regan, M. R., Haenggeli, C., Huang, Y. H., Bergles, D. E., Jin, L., Dykes Hoberg, M., Vidensky, S., Chung, D. S., et al. (2005) · Nature · doi:10.1038/nature03180 · Cited by 1,518
Self-citationSelective loss of glial glutamate transporter GLT‐1 in amyotrophic lateral sclerosis
Rothstein, J. D., Van Kammen, M., Levey, A. I., Martin, L. J., & Kuncl, R. W. (1995) · Annals of Neurology · doi:10.1002/ana.410380114 · Cited by 1,471
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Metadata
- Authors
- Rothstein, J. D., Jin, L., Dykes-Hoberg, M., & Kuncl, R. W.
- Venue
- Proceedings of the National Academy of Sciences
- Published
- 1993-07-15
- Volume
- 90
- Issue
- 14
- Pages
- 6591-6595
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- OpenAlex
- W2092034907
- Cited by
- 623
- References
- 27
- FWCI
- 25.51
- Type
- journal article
- Language
- en
- Open access
- green
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